Lines of investigation
Emerging Line of the group: “Cognition and social interactions”
Alcohol is one of the leading causes of preventable morbidity and mortality worldwide, and binge drinking represents a critical phase in the development of alcohol use disorders, particularly during periods of heightened brain plasticity. Despite its major social and health impact, relatively little is still known about the brain systems that actively limit alcohol intake and contribute to behavioral control.
Our research focuses on the study of brain circuits and specific neuronal ensembles involved in the regulation of alcohol consumption, which may constitute innate brakes on excessive drinking. We adopt an integrative approach that bridges cellular, circuit-level, and behavioral analyses. To this end, we combine animal models with activity-dependent neuronal labeling strategies (such as TRAP2 mice), causal circuit manipulation using optogenetics, in vivo functional recordings through calcium imaging and fiber photometry, as well as high-resolution transcriptomic and anatomical approaches, including single-cell RNA sequencing, MERFISH, immunofluorescence, and light-sheet microscopy. In parallel, we investigate interactions between neurons and glial cells—particularly microglia—as key modulators of synaptic plasticity associated with alcohol consumption.
Currently, the laboratory is developing several interrelated research lines: (i) the identification and characterization of neural circuits and neuronal ensembles that constrain excessive alcohol consumption; (ii) the study of how social context and prior experience shape these control mechanisms; (iii) the analysis of the role of microglia and synaptic remodeling processes in the stability of these circuits; and (iv) determining how early-life alcohol exposure influences alcohol consumption during adolescence. Together, these research lines aim to establish general principles governing the neural control of alcohol consumption and to generate knowledge with potential impact on prevention and intervention strategies.
Representative Publications
- 3,3′-Diindolylmethane attenuates recognition memory impairment induced by binge ethanol exposure in mice. Morales-Puerto N, Vidal R, Gil de Biedma-Elduayen L, Giménez-Gómez P, Núñez-de la Calle C, Trueba Y, Pérez-Hernández M, Colado MI, Gutiérrez-López MD, O'Shea E. Biochem Pharmacol. 2025 245: 117631 - PMID: 41390010 https://doi.org/10.1016/j.bcp.2025.117631
- The kynurenine pathway as a potential link between ethanol-induced behavioral alterations and neuroinflammation. Gil de Biedma-Elduayen L, Giménez-Gómez P, Morales-Puerto N, Vidal R, Del Río-García Á, Núñez-de la Calle C, Careaga L, Gutiérrez-López MD, O'Shea E, Colado MI. Front Pharmacol. 2025 16: 1628527 - PMCID: PMC12277286 https://doi.org/10.3389/fphar.2025.1628527
- Suppression of binge alcohol drinking by an inhibitory neuronal ensemble in the mouse medial orbitofrontal cortex. Gimenez-Gomez P, Le T, Zinter M, M'Angale P, Duran-Laforet V, Freels TG, Pavchinskiy R, Molas S, Schafer DP, Tapper AR, Thomson T, Martin GE. Nat Neurosci. 2025 28(8): 1741-1752 - PMID: 40495064 https://doi.org/10.1038/s41593-025-01970-x
- Dopamine control of social novelty preference is constrained by an interpeduncular-tegmentum circuit. Molas S, Freels TG, Zhao-Shea R, Lee T, Gimenez-Gomez P, Barbini M, Martin GE, Tapper AR. Nat Commun. 2024 15(1): 2891 - PMID: 38570514; PMCID: PMC10991551 doi: https://doi.org/10.1038/s41467-024-47255-y
- Oxidized soluble guanylyl cyclase causes erectile dysfunction in alcoholic mice. Olivencia MA, Gil de Biedma-Elduayen L, Giménez-Gómez P, Barreira B, Fernández A, Angulo J, Colado MI, O'Shea E, Perez-Vizcaino F. Br J Pharmacol. 2023 180(18): 2361-2376 - PMID: 37021655. https://doi.org/10.1111/bph.16087
- Modulation of neuronal excitability by binge alcohol drinking. Gimenez-Gomez P, Le T, Martin GE. Front Mol Neurosci. 2023 16: 1098211 - PMID: 36866357; PMCID: PMC9971943. https://doi.org/10.3389/fnmol.2023
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